Aureobasidium pullulans from the Fire Blight Biocontrol Product, Blossom Protect, Induces Host Resistance in Apple Flowers

Author:

Zeng Quan1ORCID,Johnson Kenneth B.2,Mukhtar Salma1,Nason Sara34,Huntley Regan1,Millet Felicia15,Yang Ching-Hong6ORCID,Hassani M. Amine1ORCID,Zuverza-Mena Nubia4,Sundin George W.7ORCID

Affiliation:

1. Department of Plant Pathology and Ecology, The Connecticut Agricultural Experiment Station, New Haven, CT 06511

2. Department of Botany and Plant Pathology, Oregon State University, Corvallis, OR 97331

3. Department of Environmental Science and Forestry, The Connecticut Agricultural Experiment Station, New Haven, CT 06511

4. Department of Analytical Chemistry, Connecticut Agricultural Experiment Station, New Haven, CT 06511

5. Department of Plant Science and Landscape Architecture, University of Connecticut, Storrs, CT 06269

6. Department of Biological Sciences, University of Wisconsin-Milwaukee, Milwaukee, WI 53211

7. Department of Plant, Soil, and Microbial Sciences, Michigan State University, East Lansing, MI 48824

Abstract

Fire blight, caused by Erwinia amylovora, is a devastating disease of apple. Blossom Protect, a product that contains Aureobasidium pullulans as the active ingredient, is one of the most effective biological controls of fire blight. It has been postulated that the mode of action of A. pullulans is to compete against and antagonize epiphytic growth of E. amylovora on flowers, but recent studies have found that flowers treated with Blossom Protect harbored similar to or only slightly reduced E. amylovora populations compared with nontreated flowers. In this study, we tested the hypothesis that A. pullulans-mediated biocontrol of fire blight is the result of induced host resistance. We found that PR genes in the systemic acquired resistance pathway, but not genes in the induced systemic resistance pathway, were induced in hypanthial tissue of apple flowers after the Blossom Protect treatment. Additionally, the induction of PR gene expression was coupled with an increase of plant-derived salicylic acid in this tissue. After inoculation with E. amylovora, PR gene expression was suppressed in nontreated flowers, but in flowers pretreated with Blossom Protect, the heightened PR expression offset the immune repression caused by E. amylovora, and prevented infection. Temporal and spatial analysis of PR gene induction showed that induction of PR genes occurred 2 days after the Blossom Protect treatment, and required direct flower–yeast contact. Finally, we observed deterioration of the epidermal layer of the hypanthium in some of the Blossom Protect-treated flowers, suggesting that PR gene induction in flowers may be a result of pathogenesis by A. pullulans.

Funder

U.S. Department of Agriculture, National Institute of Food and Agriculture, Organic Transitions

U.S. Department of Agriculture, National Institute of Food and Agriculture, Agricultural Microbiome

Lou Magnarelli Postdoctoral Fellowship

New England Tree Fruit Growers Research Committee

Publisher

Scientific Societies

Subject

Plant Science,Agronomy and Crop Science

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